Impaired acid stress resistance in Salmonella Typhi Ty2

preprint OA: closed
Full text JSON View at publisher
AI-generated summary by claude@2026-07, 2026-07-14

Salmonella Typhi Ty2 exhibits impaired acid stress resistance compared to S. Typhimurium due to genomic decay and loss of essential acid survival genes, while heterologous gene expression restores acid tolerance.

One-sentence paraphrase of the abstract; not a substitute for reading it. No clinical advice. How this works

AI-generated deep summary by claude@2026-07, 2026-07-14 · read from full text

The paper studied how two Salmonella enterica serovars, S. Typhimurium 14028s and the human-adapted S. Typhi Ty2, respond to acid stress by comparing growth across pH 3–8 and performing transcriptomic profiling at pH 4.5 versus 7.5. S. Typhimurium showed enhanced growth at pH 4.5, and transcriptomics identified acid-induced differentially expressed genes including membrane proteins (OmpC, PhoE, HydB), a regulator (RpoS), and stress response proteins (YciG, STM14_1829, YmdF). Targeted deletion of selected genes in S. Typhimurium suppressed growth at acidic pH, while these acid-resistance functions were compromised in S. Typhi due to pseudogenization, and restoring expression of pseudogenized genes recovered acid tolerance; a key limitation is that the experiments focus on pH and gene functions rather than in vivo infection outcomes. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

Read from the paper's body, not the abstract. Not a substitute for reading the paper. No clinical advice. How this works

Abstract

Salmonella enterica encounters acid stress during gastrointestinal transit and within the phagosomal environment of macrophages. Acid stress resistance has been well characterized in Salmonella enterica serovar Typhimurium, but comparative studies in the human-adapted Salmonella enterica serovar Typhi are limited. We compared the growth of S. Typhimurium 14028s and S. Typhi Ty2 at pH values ranging from 3-8 and observed that Salmonella enterica serovar Typhimurium exhibits enhanced growth at pH 4.5 compared to S. Typhi. Comparative transcriptomic profiling of S. Typhimurium and S. Typhi at pH 4.5 and 7.5 identified numerous differentially expressed acid-induced genes (DEGs), including genes encoding membrane proteins (OmpC, PhoE, HydB), a transcriptional regulator (RpoS), and stress response proteins (YciG, STM14_1829, YmdF). Targeted deletion of selected genes in S. Typhimurium significantly suppressed growth at acidic pH, confirming their role in acid stress resistance. These resistance mechanisms are compromised in S. Typhi due to pseudogenization. Heterologous expression of pseudogenized genes in S. Typhi restored acid tolerance. Collectively, these findings suggest that S. Typhi has lost the ability to withstand acid stress due to genomic decay and the loss of multiple genes essential for acid survival in S. Typhimurium, reflecting divergent evolutionary paths in these two serovars. Importance Salmonella Typhimurium must adapt to acidic pH conditions in the intestinal tract and the intracellular environment to cause infection. In this study, we show that the enteric fever serovar Salmonella Typhi exhibits impaired growth at pH 4.5, in comparison to Salmonella Typhimurium. We further show that the loss of specific membrane proteins, a transcriptional regulator, and a family of stress response proteins in Salmonella Typhi are responsible for this difference. Collectively, these observations suggest that Salmonella Typhi has evolutionarily lost the ability to withstand acid stress due to differences in its interaction with the human host. This has important implications for the pathogenesis of typhoid fever.
Full text 2,156 characters · extracted from oa-doi-fallback · click to expand
Abstract Salmonella enterica encounters acid stress during gastrointestinal transit and within the phagosomal environment of macrophages. Acid stress resistance has been well characterized in Salmonella enterica serovar Typhimurium, but comparative studies in the human-adapted Salmonella enterica serovar Typhi are limited. We compared the growth of S. Typhimurium 14028s and S. Typhi Ty2 at pH values ranging from 3-8 and observed that Salmonella enterica serovar Typhimurium exhibits enhanced growth at pH 4.5 compared to S. Typhi. Comparative transcriptomic profiling of S. Typhimurium and S. Typhi at pH 4.5 and 7.5 identified numerous differentially expressed acid-induced genes (DEGs), including genes encoding membrane proteins (OmpC, PhoE, HydB), a transcriptional regulator (RpoS), and stress response proteins (YciG, STM14_1829, YmdF). Targeted deletion of selected genes in S. Typhimurium significantly suppressed growth at acidic pH, confirming their role in acid stress resistance. These resistance mechanisms are compromised in S. Typhi due to pseudogenization. Heterologous expression of pseudogenized genes in S. Typhi restored acid tolerance. Collectively, these findings suggest that S. Typhi has lost the ability to withstand acid stress due to genomic decay and the loss of multiple genes essential for acid survival in S. Typhimurium, reflecting divergent evolutionary paths in these two serovars. Importance Salmonella Typhimurium must adapt to acidic pH conditions in the intestinal tract and the intracellular environment to cause infection. In this study, we show that the enteric fever serovar Salmonella Typhi exhibits impaired growth at pH 4.5, in comparison to Salmonella Typhimurium. We further show that the loss of specific membrane proteins, a transcriptional regulator, and a family of stress response proteins in Salmonella Typhi are responsible for this difference. Collectively, these observations suggest that Salmonella Typhi has evolutionarily lost the ability to withstand acid stress due to differences in its interaction with the human host. This has important implications for the pathogenesis of typhoid fever.

Text is read by the "Ask this paper" AI Q&A widget below. Extraction quality varies by source — PMC NXML preserves structure cleanly, OA-HTML may include some navigation residue, and OA-PDF can have broken hyphenation. The publisher copy (via DOI) is the canonical version.

My notes (saved in your browser only)

Ask this paper AI returns verbatim quotes from the full text · source: oa-doi-fallback

Answers must be backed by verbatim quotes from this paper's full text. Hallucinated quotes are dropped automatically; if no verbatim passage answers the question, we say so. How this works

Citation neighborhood (no data yet)

We don't have any in-corpus citations linked to this paper yet. This is a recent paper (2026) — citers typically take a year or two to land, and the OpenAlex reference graph may still be filling in.

Source provenance

europepmc
last seen: 2026-05-20T01:45:00.602351+00:00